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Interactions Between Environmental and Genetic Factors in the Pathophysiology of Parkinson's Disease
Author(s) -
Tsang Fai.,
Soong Tuck Wah
Publication year - 2003
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/1521654031000153058
Subject(s) - dopaminergic , neuroprotection , parkinson's disease , oxidative stress , disease , neuroscience , mptp , pathophysiology , dopamine , ferritin , biology , transgene , population , genetically modified mouse , neurodegeneration , genetic predisposition , mechanism (biology) , medicine , genetics , gene , endocrinology , biochemistry , philosophy , environmental health , epistemology
Parkinson's disease (PD) is a progressive neurodegenerative disease with no known cure and affects approximately 1% of the elderly population. The major question in PD relates to the selective loss of dopaminergic neurons in patients. The underlying mechanism of genetic dysfunction and environmental toxins in contributing to the pathogenesis of PD may be oxidative stress. The interactions of genetic and environmental factors in PD may provide some answers to the longstanding question. In particular, the possibility that iron may provide selectivity to genetic susceptibility or dopamine reactivity in dopaminergic neuronal death is enhanced by the neuroprotection demonstrated in transgenic mice overexpressing ferritin or the use of iron chelators in MPTP‐induced PD mouse. It will be important to dissect and understand the contributions of genes, environment and intrinsic cellular states in the generation and progression of the pathophysiology of PD. IUBMB Life, 55: 323‐327, 2003